The overall goal of this R01 and its companion IRPG proposals is to determine if there is altered dopamine neurotransmission in high risk nonalcoholics which predates the development of alcoholism and whether this dopaminergic defect is further deranged by chronic alcoholism. This R01 will examine dopamine release in chronic alcoholics and controls with PET scanning procedures and will relate this information to response to a Naloxone challenge. The investigators propose a model that alcoholism results from a deficiency of mesolimbic dopamine D2 receptors. An individual's low D2 receptor activity can be the result of genetic variance in the D2 receptor itself caused by the presence of the A1 D2 receptor allele, down regulation secondary to increased dopamine release secondary to stress-induced hypercortisolemia due to an anxious/depressed personality type or novelty seeking behavior, and the toxic effects of alcohol abuse per se. If the initial D2 receptor deficits are exacerbated by alcohol abuse one can envision a positive feedback loop hard to break.